Acacetin inhibits expression of E-selectin on endothelial cells through regulation of the MAP kinase signaling pathway and activation of NF-κB

Naomi Tanigawa, Makoto Hagiwara, Hiroyuki Tada, Toshinori Komatsu, Shinsuke Sugiura, Kaoru Kobayashi, Yoshiko Kato, Naoyuki Ishida, Kyohei Nishida, Masayuki Ninomiya, Mamoru Koketsu, Kenji Matsushita

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)

Abstract

Since E-selectin-mediated adhesion of leukocytes or tumor cells to the vascular endothelium is a key early event in the initiation of inflammatory response and cancer metastasis, E-selectin inhibition is thought to be a good target for therapeutic intervention. Several flavones have been shown to have anti-inflammatory and anticancer properties. In the present study, we investigated the effects of plant flavones on expression of E-selectin in human umbilical vein endothelial cells. Among 11 flavones, acacetin strongly inhibited TNF-α-induced E-selectin expression in HUVECs. Acacetin suppressed the TNF-α-induced phosphorylation of p38 but did not inhibit TNF-α-induced phosphorylations of JNK and ERK. Acacetin also inhibited the activation of NF-κB by stimulation with TNF-α. Furthermore, adhesion of monocytes to TNF-α-treated endothelial cells was inhibited by cotreatment with acacetin. These results suggest that acacetin inhibits the expression of E-selectin by regulation of the p38 MAPK signaling pathway and activation of NF-κB.

Original languageEnglish
Pages (from-to)471-477
Number of pages7
JournalImmunopharmacology and Immunotoxicology
Volume35
Issue number4
DOIs
Publication statusPublished - 2013 Aug 1
Externally publishedYes

Keywords

  • Adhesion molecules
  • Flavones
  • Immunomodulation
  • Supplement
  • Vascular inflammation

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Toxicology
  • Pharmacology

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